缬沙坦
内科学
医学
心脏病学
肥厚性心肌病
沙库比林、缬沙坦
沙库比林
心功能曲线
舒张期
心肌病
心力衰竭
内分泌学
血压
作者
Jovana Jeremić,Natalia Govoruskina,Jovana Bradić,Isidora Milosavljević,Ivan Srejović,Vladimir Živković,Nevena Jeremić,Tamara Nikolic Turnic,Irena Tanasković,Stefani Bolevich,Vladimir Jakovljević,Sergey Bolevich,Marko Živanović,Nduka Okwose,Dragana Šeklić,Nevena Milivojević,Jelena Grujić,Lazar Velicki,Guy MacGowan,Djordje G Jakovljevic,Nenad Filipović
标识
DOI:10.1007/s11010-023-04690-7
摘要
This study evaluated the effect of sacubtril/valsartan on cardiac remodeling, molecular and cellular adaptations in experimental (rat) model of hypertension-induced hypertrophic cardiomyopathy. Thirty Wistar Kyoto rats, 10 healthy (control) and 20 rats with confirmed hypertension-induced hypertrophic cardiomyopathy (HpCM), were used for this study. The HpCM group was further subdivided into untreated and sacubitril/valsartan-treated groups. Myocardial structure and function were assessed using echocardiography, Langendorff's isolated heart experiment, blood sampling and qualitative polymerase chain reaction. Echocardiographic examinations revealed protective effects of sacubitril/valsartan by improving left ventricular internal diameter in systole and diastole and fractional shortening. Additionally, sacubitril/valsartan treatment decreased systolic and diastolic blood pressures in comparison with untreated hypertensive rats. Moreover, sacubitril/valsartan treatment reduced oxidative stress and apoptosis (reduced expression of Bax and Cas9 genes) compared to untreated rats. There was a regular histomorphology of cardiomyocytes, interstitium, and blood vessels in treated rats compared to untreated HpCM rats which expressed hypertrophic cardiomyocytes, with polymorphic nuclei, prominent nucleoli and moderately dilated interstitium. In experimental model of hypertension-induced hypertrophic cardiomyopathy, sacubitril/valsartan treatment led to improved cardiac structure, haemodynamic performance, and reduced oxidative stress and apoptosis. Sacubitril/valsartan thus presents as a potential therapeutic strategy resulted in hypertension-induced hypertrophic cardiomyopathy.
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